INFLAMMATORY

LESIONS OF THE
JAW
Dr. Bhavika pol vhatkar
1st yr pg
 OSTEOMYELITIS

OSTEORADIONECROSIS

PERICORONITIS

OSTEOSCLEROSIS
INTRODUCTION

“Osseous” in Latin means – Bony

“Osteon” in Greek means – Bone

“myelos” means Marrow

“itis” means inflammation

Osteomyelitis is an inflammation of medullary portion

of bone or bone marrow.
3
 DEFINITION :
• Osteomyelitis is an extensive inflammation
of a bone. It involves the cancellous
portion, bone marrow, cortex, and
periosteum.(Laskin 1989)

• Osteomyelitis is defined as an inflammatory

condition of bone primarily involving the
soft tissues (Archer)

• Osteomyelitis is an inflammation of bone

marrow with a tendency to progression. It
involves adjacent cortical plates and often
periosteal tissues. (Michael Miloro 2004)
4
“OSTEOMYELITIS IS AN INFLAMMATORY
CONDITION OF THE BONE THAT BEGINS
AS AN INFECTION OF THE MEDULLARY
CAVITY AND HAVERSIAN SYSTEMS AND
EXTENDS TO INVOLVE THE CORTICAL
BONE AND THE PERIOSTEUM OF THE
AFFECTED AREA”
 BONE – NORMAL ANATOMY

Lamellae – weight-bearing,
Osteon/ Haversian system –
column-like matrix tubes
the structural unit of
composed of collagen and
compact bone.
crystals of bone salts.

Volkmann’s Canals – channels

lying at right angles to the
Haversian Canal – central
central canal, connecting blood
channel containing blood
and nerve supply of the
vessels and nerves.
periosteum to the Haversian
canal
6
 CLASSIFICATION
 Historically accepted classification –
[HUDSON’S CLASSIFICATION]

I. ACUTE –
a. Contiguous focus – trauma, surgery &
odontogenic infections
b. Progressive – burns, sinusitis, vascular
insufficiency
c. Hematogenous – metastatic (children)

7
II CHRONIC

a. Recurrent multifocal – developing skeleton,

escalated osteogenic activity (<25 years)

b. Garre’s – (i)unique proliferative subperiosteal

reaction, (ii) Developing skeleton (children to
young adults)

c. Suppurative or non suppurative – (i) inadequately

treated forms , (ii) systemically compromised,
(iii) refractile

d. Diffuse sclerosing – (i) fastidiouis organisms, (ii)

compromised host pathogen interface
8
 CLASSIFICATION BASED ON
PATHOGENESIS OF ALTERED
VASCULAR PERFUSION
 Proposed by VIBHAGOOL ET AL (1993)

I. Hematogenous osteomyelitis

II. Osteomyelitis secondary to contiguous

focus of infection

III.Osteomyelitis associated with or without

peripheral vascular disease
9
 CLASSIFICATION GIVEN BY ANDERSON
I) Acute suppurative

II) Chronic suppurative

- without prior acute osteomyelitis (primary)
- with prior acute osteomyelitis (secondary)

III) Chronic non suppurative

- Focal sclerosing (condensing)
- Diffuse sclerosing
- With proliferative periostitis (Garre’s)

10
IV) Actinomycotic

V) Syphilitic

VI) Tuberculous

VII) Sterile (osteoradionecrosis)

11
ETIOLOGY
• Pulp pathosis
• Periodontal Diseases
• Pericoronitis
• Infective cyst and tumour
Local •
•
Infected extraction socket
Infected jaw fracture
Factors • Infected soft tissue injury
• Peritonsilar abscess
• Periostitis following gingival
ulceration
 ETIOLOGY
• Systemic Tuberculosis
• URT infection
• Middle ear infection
Haematogenous • Mastoiditis
Factors • Furuncle of the face
• Wound on the skin
• Local
• Haematogenous
 PREDISPOSING
FACTORS:
Low resistance
• Diabetes
• Agranulocytosis
• Tb, syphilis, typhoid, aids,
• Leukemia
• On steroids
Factors affecting the vascularity of the bone
• Paget’s disease
• Fibrous dysplasia
• Radiation
• Osteopetrosis
• Bone malignancy
• Bone necrosis
 PATHOGENESIS
Virulent Organisms reach the depth of the bone and
set up an inflammatory reaction

Infection spreads rapidly through the bone and

reaches the cortex

Perforates the cortex and reaches the undersurface of

the periosteum

At this stage, it Spreads subperiosteally over the

surface of the bone

Pus enters the depth of the bone from a different site

through the Volkman’s canals
 Blood vessels in the canal show stasis of blood followed by
thrombosis and embolism

Due to thrombosis, the part of the bone undergoes necrosis and

forms the sequestrum

Infection spreads within the bone and also subperiosteally

Periosteum is stimulated in the involved region to form new bone

called involucrum
Function of the involucrum is to join
the two living fragments of the bone
and maintain the integrity of the bone

On the surface of the bone, small

orifices are formed called cloacae
through which the pus drains out

After removal of the sequestrum,

resorption of the involucrum takes
place and bone may recover its
original shape
Formation of a sequestrum:
(A), sound bone;
(B), new bone;
(C), granulations lining involucrum;
(D), cloaca;
(E), sequestrum.
 CLINICAL FEATURES
 Mandible > Maxilla
 High fever
 Tachycardia, increased respiratory rate
 Nausea, vomitting, dehydration
 Leucocytosis
 lymphadenopathy
 Fluctuant abscess or cellulitis
 Swelling, tender, redness, severe pain
 Multiple discharging sinuses
 Mobiltiy of the tooth, pain on percussion
 Trismus
 Fetid oral odour
 Paraesthesia of the lip
 Intraorally, bare bone maybe seen
 ACUTE OSTEOMYELITIS
 Rapid onset and course
 Few radiographic signs

Clinical features:
 Extreme pain
 Regional lymphadenopathy
 Soreness of involved tooth, mobile
 Paresthesia or anesthesia of lip
 Swelling not apparent
 WBC count and temperature should be evaluated
 Reflex spasm of muscles attached to that part of bone
Acute osteomyelitis involving the body of the right mandible,
with initial blurring of bony trabeculae.
` RADIOGRAPHIC
FEATURES:
About 10 days after bone involvement:

Decreased trabecular density

Blurred and fuzzy outlines

Solitary or multiple radiolucencies- enlarged

marrow spaces due to focal necrosis and bone
destruction
 ACUTE SUBPERIOSTEAL
 OSTEOMYELITIS
Mandibular periapical abscesses
 Invade cortex and reach subperiosteal space
 Erosion of cortex
 Pus ruptures through intraoral and extraoral draining
sinuses.
Clinical features:
 Severe pain
 Intraoral and extraoral swelling
 Regional lymphadenitis
 Tooth only mildly sensitive to percussion
 Intraoral and extraoral sinuses
Radiographic features:
 Occlusal radiograph: erosion of cortex
 No extensive involvement of adjacent
cancellous bone
CHRONIC OSTEOMYELITIS

 May be sequelae to acute phase

 May be the first to occur: virulence- host
response
 Milder symptoms
 Bone destruction slower
 Patient more comfortable
CT image of multiple sequestra. A, An axial scan (bone
window) revealing multiple sequestra (arrows)
An axial CT image using bone window of the mandible. Note the increase in bone
density, width of the mandible, and the new periosteal bone formation (white arrow)
and evidence of the original cortex (black arrow).
CHRONIC SUPPURATIVE
OSTEOMYELITIS
 Infection is localized but persistent
 Milder symptoms
 May be single or multiple, may be present for a
variable period, upto years, with periods of
exacerbation.
Clinical features:
 Local tenderness and swelling over bone
 Mild leucocytosis and regional lymphadenopathy
 Low grade fever
 Sinuses- drain pus and close
 Radiographic features:

 Single or multiple radiolucencies of variable size,

irregular, poorly defined
 Moth eaten appearance
 Sequestra: irregular calcified areas seperated from the
remaining bone.
 Fistulous radiolucent tract to the surface.
Chronic suppurative osteomyelitis with three
sequestra (arrows). Osteolytic as well as sclerotic
areas are present.
Suppurative osteomyelitis
Sequestrum
DIFFUSE SCLEROSING
OSTEOMYELITIS
 Balance between virulence and resistance.
 Reactive proliferation of bone
 Focal or diffuse
 Diffuse: any age but common in older age
groups.
 Confined to Mandible, but Maxilla, femur,
tibia, fibula may be involved.
 Clinical features:

 Symptoms: mild or absent

 Jaw enlarged on affected side
 Pain and tenderness during periods of growth
 F>M
 High ESR and fever
 May show improvement with long term antibiotics
 Decortication effective in relieving pain and
decreasing frequency
 Cortisone injection: blocking episodes of pain
Chronic sclerosing osteomyelitis of right mandible with some
osteolytic areas. Ramus is enlarged.
 a b

a) Right mandibular molars in a young patient. The alveolar bone is

unevenly sclerotic; chronic sclerosing osteomyelitis.
b) Occlusal view of the same patient. Periosteal bone formation (arrow) on
the buccal side of the mandible.
Radiographic features:
 Early: diffuse osteolytic and osteosclerotic zones
 Later: more sclerotic
 Luscent areas may be identified.

D/D:
 Osteosarcoma, metastatic osteoblastic carcinoma,
pagets, chondrosarcoma.
FOCAL SCLEROSING OSTEOMYELITIS
39
(condensing osteitis)
 Unusual reaction of bone to infection.

 Reaction to mild bacterial infection entering

the bone through a carious tooth in persons
who have high degree of tissue resistance &
tissue reactivity.

 Tissue reacts to infection by proliferation

rather than destruction.
CLINICAL FEATURES 40

 Most commonly in children and young adults,

rarely in older individuals.

 Tooth most commonly involved is the

mandibular third molar presenting with a large
carious lesion.

 Nosigns or symptoms other than mild pain

associated with infected pulp.
RADIOGRAPHIC FEATURES 41

 Pathognomic, well circumscribed radiopaque mass of

sclerotic bone surrounding & extending below apex of
one or both roots.

 Entire root outline always visible with intact lamina

dura.

 Periodontal ligament space widened.

 Border smooth & distinct appearing to blend into

surrounding bone
RADIOGRAPHIC FEATURES 42
RADIOGRAPHIC FEATURES 43
TREATMENT & PROGNOSIS 44

 Affected tooth may be treated endodontically

or extracted.
 Scleroticbone not attached to tooth and
remains behind after tooth is removed.
 This dense area may not get remodeled.
 Recognizable on bone years later and is
referred as bone scar.
D/D FOR FOCAL SCLEROSING
45

OSTEOMYELITIS
 Benign cementoblastoma

 Florid cemento osseous dysplasia

 Osteosarcoma (osteoblastic variant)

 Odontoma (rare cases)

CHRONIC SUBPERIOSTEAL
OSTEOMYELITIS
 Sequelae of acute
 Following drainage of pus.
 Cortex becomes necrotic, and multiple small sequestra
are formed.
 Sequestra act as foreign body and perpetuate a
suppurative process and are eventually discharged
through multiple sinuses that are formed.
 After this healing occurs rapidly.
 • Slight pain
Clinical • Regional lymphadenitis
• Swelling confined to sulcus
features:
• Multiple draining sinuses

• Moth eaten appearance of

intramedullary osteomyelitis
Radiographic • Occlusal: cortical sequestration:
multiple small radiopaque flakes
features: • Mottled appearance of adjacent
trabecular bone
Clinical picture 48

 Osteomyelitis
affecting the maxilla

 Bone destruction
seen intra orally
 RADIOGRAPHIC PICTURE 49

 Characteristic moth eaten appearance

 Presence of sequestra
RADIOGRAPHIC PICTURE 50

 Characteristic moth eaten appearance

 GARRE’S OSTEOMYELITIS
 Rare, non suppurative sclerosing osteomyelitis of the jaws
characterized by formation of hard bony swelling on the surface of
jaws.
 Mild infection from cancellous portion.
Clinical features:
 Hard non tender swelling
 Inferior mandible, medial or lateral involvement also present
 F>M
 <30 yrs
 Mandible>Maxilla
 Mass: 1-2 cm or entire length on affected side
 Pain before enlargement of jaw occurs.
 Secondary infection: discomfort
Radiographic features:

 A shadow of thin convex shell of bone over cortex

 No trabeculation between the shell and cortex
 As infection proceeds, cortex becomes laminated:
onion peel appearance
 Adjacent cancellous bone may be normal, sclerotic or
osteolytic.
 After removal of irritation, cortical bone remodels

D/D:
 Ewings sarcoma, infantile cortiical
hyperostosis,Fibrous dysplasia, osteomas,
osteosarcoma
A and B, Proliferative periostitis resulting from infl ammatory
lesions. Note the multiple layers of new bone on the buccal
aspect of the mandible, resulting in an onion-skin appearance.
 MANAGEMENT

 Tends to be more difficult to eradicate than

acute form.
 Hyperbaric oxygen therapy and creative
modes of long term antibiotic delivery have
been used.
 Surgicalintervention- sequestrectomy,
decortication or resection is often
necessary.
INFECTIVE
OSTEOMYELITIS
Tuberculous
osteomyelitis

Syphilitic
osteomyelitis

Actinomycotic
osteomyelitis
56
 Tuberculous osteomyelitis
 Results when blood borne bacilli lodge in cancellous
bone.

 Usually commences in metaphyseal area of long

bones & causes widespread destruction of osseous
tissue.

 Commonly seen in phalanges and dorsal and lumbar

vertebrae.

 Tuberculous lesions are rare in jaws.

57
PATHOGENESIS
• Direct inoculation – through an
ulcer or break in mucosa
• Spread to bone via an extraction
Three socket or infected fracture line
possible • Hematogenous or lymphatic spread
methods of from a primary focus elsewhere in
inoculation body.
of bacteria
into the
bone

58
Usually occurs secondary to tuberculosis of
lungs.

Cases have been reported where mandibular

lesions were not associated with pulmonary
disease.

Darlington proposed that infection may

spread to the underlying bone from a
surface lesion in the jaws.

Another common entrance is through a

carious tooth via open pulp.

59
Progresses slowly, with the formation of
tubercle in bone marrow.

Increased vascularity of periosteum with initial

subperiosteal resorption of bone, followed by
laying down of new layer of reactive bone.

As disease progresses, there is caseation in

central portion of bone.

Ultimately pus extends peripherally & a

subperiosteal abscess is formed.

60
If disease still progresses, periosteum gives
way & tuberculous debris are expelled into
soft tissues.

Infection tracks along the fascial planes to

the surface of skin.

Abscess reddens but is not warm (cold

abscess)

Skin becomes progressively thinner &

ultimately yields to form a tubercular sinus.

61
 CLINICAL FEATURES
 Sites most commonly involved are ramus & body of
mandible.

 Age group affected is around 15 – 40 years.

 Patient may show features similar to subperiosteal

abscess, which may initially be drained resulting in
non healing sinus tract formation.

62
 Closed lesions

 Lesion located centrally in bone

 Patient presents with only swelling & no draining

sinuses.

 Usually absence of any oral septic foci

 Usually in ramus, may mimic parotid swelling or

submassetric abscess.

63
 Open lesions –

 Presence of multiple extraoral & intraoral sinuses

with mucopurulent discharge.

 Oral septic foci may or may not be present.

64
 RADIOGRAPHIC FEATURES

 Non characteristic, most lesions

indistinguishable from those caused by
pyogenic organisms.

 Lesions either localized resembling rarefying

osteitis, or maybe diffuse.

 Subperiosteal bone formation not common,

unless superimposed secondary infection.

65
 Unilateral diffuse swelling Lower left buccal vestibule
on left side of mandible obliterated from 74 to 36
with draining sinus

66
 Ill defined radiolucent Occlusal view showing
osteolytic lesion periosteal reaction

67
 SYPHILITIC OSTEOMYELITIS
Difficult to distinguish syphilitic osteomyelitis of the jaws from
pyogenic osteomyelitis on clinical & radiographic examination.

Main features are progressive course & failure to improve with

usual treatment for pyogenic osteomyelitis.

Massive sequestration may occur resulting in pathologic

fracture.

If unchecked, eventually causes perforation of the cortex.

Identity of the organism may be masked due to superimposed bacterial

infection. 68
 ACTINOMYCOTIC
OSTEOMYELITIS

 Actinomyces – generic term applied to group

of non acid fast organisms that are
microaerophilic.

Three species –
i. Actinomyces israeli – primarily saprophytic,
occasionally pathogenic.
ii. Actinomyces bovis – in cattle
iii. Actinimyces baudetti – cats and dogs

71
 Pathogenesis
The organisms thrive in the oral cavity, especially tissues adjacent
to mandible.

May enter the bone through a fresh wound, carious tooth or a

periodontal pocket at the gingival margin of erupting tooth.

Following entry of the organism there is a protracted incubation

period, after which a swelling appears.

Infection spreads without regard to fascial planes & typically

appears on cutaneous rather than mucosal surfaces.
72
 Clinical features
 Soft or firm tissue masses on skin, which have
purplish, dark red, oily areas with occasional zones
of fluctuation.

 Spontaneous drainage of serous fluid containing

granular material.

 Regional lymph nodes occasionally enlarged.

 Trismus not common, unless secondarily infected.

73
 According to Aird, mandible may be affected as follows
–

 Periostitis – after involvement of overlying soft parts

 Actinomycotic osteomyelitis – mandible greatly

thickened & honeycombed by narrow tracks containing
the organisms.

 Central rarefying osteomyelitis – very rare, result of

infection gaining entry to the cancellous tissue &
producing area of rarefaction

74
 Radiographic features
 No specific radiographic features

 May appear as a radiolucency varying in size from that

of apical granuloma to extensive involvement of bone.

 Osteolytic process is accompanied either by marked

thickening & sclerosis of the jaw or osteoblastic
reaction is absent or minimal.

 If teeth are adjacent to the site of bone destruction,

their lamina dura may be deficient apically or roots
resorbed slightly.

75
 Differential Diagnosis

Parotitis

Parotid tumors

Cervical tuberculosis

Pyogenic osteomyelitits
77
 TREATMENT 78

CONSERVATIVE METHOD:

 Systemic antibiotics
 Selective rinsing with topical antiseptics
 Selective removal of small sequestra
 Curetting & local debridement
 Burring of bone until normal bleeding bone
appears.
 79

RADICAL TREATMENT

 Directed to supporting & salvaging viable but

compromised tissue.

 Reversing hypoxia & increasing the

vascularity & cellularity.
 Steps involved are -
80

 Debridement
 Control of infection
 Hospitalisation
 Hydration & nutritional supplements
 Analgesics
 Maintaining good oral hygiene
 Frequent irrigation of wounds
 Removal of exposed dead bone
 Sequestrectomy
 Bone resection
 Hyperbaric Oxygen therapy
 MALIGNANCY IN 81

 OSTEOMYELITIS
Patients having long standing chronic osteomyelitis with a
sinus tract may develop malignancy.

 Nearly always low grade squamous cell carcinoma.

 Patients complain of increased foul smelling discharge &

pain.

 Clinically white cauliflower like growth on the sinus tract.

 Due to papillary projections on the surface covered with

keratin
 82

 Histologically, may be so well differentiated

that it may be difficult to make diagnosis of
carcinoma.

 Presence of squamous epithelium in bone

should be taken as sign of definitive
malignancy.

 Treatment is amputation/ resection

COMPLICATIONS IN
OSTEOMYELITIS 83

 Neoplastic transformation

 Discontinuity defects

 Progressive diffuse sclerosis

 Cavernous sinus thrombosis

 investigations 84

 CULTURE & SENSITIVITY TESTS

 STAINING & MICROSCOPY
 BLOOD INVESTIGATIONS
 BONE MARROW ASPIRATION
 IMAGING
 Culture & Sensitivity Tests 85

 BLOOD CULTURES
AGAR MEDIUM

 ANEROBIC CULTURE MEDIA

ROBERTSON’S COOKED MEAT MEDIA
 M. TUBERCULOSIS
LOWENSTEIN JENSON MEDIA
 Staining & Microscopy 86

 GRAM STAINING

 ACID FAST STAINING

 FUNGAL STAINING

 DARK FIELD MICROSCOPY

 Blood Investigations 87

 COMPLETE HEMOGRAM
HEMOGLOBIN
TOTAL COUNT
DIFFERENTIAL COUNT
ESR
 PERIPHERAL BLOOD SMEAR
 BLOOD SUGAR
 Imaging 88

CONVENTIONAL
 IOPA
 OCCLUSAL
 OPG
 LATERAL OBLIQUE
 OTHER EXTRA ORAL RADIOGRAPHS
 89

ADVANCED
 BONE SCAN
 CT SCAN
 MRI
 POSITRON EMISSION TOMOGRAPHY
 TREATMENT 90

 Goal of management is –
- Attenuate & eradicate proliferating
pathological organisms
- Promote healing
- Re- establish vascular permeability
 Management includes –
 Conservative management
 Surgical management
Treatment guidelines 91

 DISRUPT THE INFECTIOUS FOCI

 DEBRIDEMENT
 CULTURE & SENSITIVITY TESTS
 DRAINAGE & IRRIGATION
 BEGIN EMPIRIC ANTIBIOTIC THERAPY
 STABILIZATION
 CONSIDER ADJUNCTIVE TREATMENTS
 RECONSTRUCTION
( MARX. 1992)
 Conservative Management 92

 Complete bed rest

 Supportive therapy

 Rehydration

 Blood transfusion

 Pain control

 Antimicrobial therapy
93
 Hyperbaric Oxygen Therapy 94

 Involves intermittent, usually daily, inhalation of

100% humidified oxygen under pressure greater than
1 absolute atmospheric pressure

 Patient is placed in a chamber, oxygen is given by

mask or hood

 Each session, or dive, is 90 minutes in length.

 Treatment given 5 days per week for 30, 60 or more

dives at 2.4 ATp for 90 minutes while breathing 100%
oxygen twice daily
 Beneficial aspects of hyperbaric oxygen
95

 Enhancement of lysosomal degradation potential of

PMLs and oxygen radicals.

 Free radicals of oxygen bactericidal to many

pathogens.

 Many exotoxins liberated by microorganisma rendered

inert by exposure to elevated partial pressure of
oxygen.

 Tissue hypoxia intermittently reversed by HBO

mimicking tissue level during wound healing

 Positive enhancement of neo-angiogenesis

HBO
CHAMBER
96
 Contraindications 97

 As considered by the HBO Committee of the

Undersea Medical Society, Fisher et al(1988) & Marx
et al (1985)
 Pneumothorax
 Severe COPD
 Optic neuritis
 Acute viral infection
 Upper respiratory tract infection
 Congenital spherocytosis
 Uncontrolled acute seizures
 Malignant disease
 Surgical Therapy 98

 Incision & drainage

 Extraction of loose teeth
 Debridement
 Decortication
 Sequestrectomy
 Saucerization
 Trephination or fenestration
 Resection
 Immediate/ delayed reconstruction
 Postoperative care
 HUDSON’S OSTEOMYELITIS 99

TREATMENT PLAN
 FOR ACUTE ASTEOMYELITIS

Healthy host
 Conservative decompression & debridement
with extraction
 Drainage & irrigation if pus present
 Culture & sensitivity of infected foci
 Antibiotic treatment for 3 – 4 weeks
 Regional bony stabilization if necessary
Compromised Host 100

 Stabilize condition – especially nutrition

 Aggressive debridement & decompression
with disruption of involved periosteal
layer
 Culture & sensitivity of infected foci
 Sustained antibiotic treatment for 6 – 12
weeks
 Regional bony stabilization if necessary
 FOR CHRONIC OSTEOMYELITIS 101

 Host almost always compromised.

 CT, nuclear medicine scan, bone perfusion

 Stabilize condition of host especially

nutrition status

 Wide bony sequestrectomy & decortication

to normal bleeding bone
 102

 If purulent, consider drainage & irrigation

 Sustained antibiotic therapy for 3 – 6 months

 Regional bony stabilization

 Postoperative HBO – 20- 40 dives for 90 min at

2.5 ATA

 Reconstruction as necessary
OSTEORADIONECROSIS
 OSTEORADIONECROSIS
 Inflammatory condition of bone that occurs after the
bone has been exposed to therapeutic doses of radiation,
usually given for a malignancy of the head and neck
region.
 Characterized by presence of exposed bone for at least
3 months occurring at any time after the administration
of therapeutic radiation.
 Doses above 50 Gy are usually required to cause this
condition.
 Bone is hypocellular and hypovascular
 Hypovascularity results in hypoxic environment in which
adequate healing of bone is not possible.
CLINICAL FEATURES
 Mandible > Maxilla
 Posterior Mandible > anterior Mandible
 Posterior body of Mandible is more frequently
in the direct field of radiation treatment
because primary tumors and metastatic lesions
in the lymph nodes being treated are adjacent
to this part of mandible.
 Loss of mucosal covering and exposure of bone
is the hallmark
 Pathologic fracture may occur.
106
 The exposed bone becomes necrotic due to
loss of vascularity from the periosteum and
later sequestrates, leading to exposure of
more bone.
 Pain may or may not be present.
 Intense pain may occur, with intermittent
swelling and drainage extraorally.
 However, many patients experience no pain
with bone exposure.
 RADIOGRAPHIC FEATURES
 Similar to those of chronic osteomyelitis.
 Location:
 Mandible

 Posterior mandible
 Maxilla, sometimes.

• Periphery:
 Ill defined, similar to that in osteomyelitis.
 If the lesion reaches inferior border, irregular bony
resorption occurs.
 A B

Osteoradionecrosis of the maxilla. These periapical filmswere taken before radiotherapy

(A) and within 6 months of receiving the radiation (B) . Note the combination of bone
sclerosis and profound bone destruction around the teeth and alveolar crest and
widening of the periodontal membrane space
Radiologic features 110
An axial CT image showing a well-defi ned region of cortical bone resorption
(arrow), an early change in therapeutic radiation exposure.
 Internal structure:
A range of bone formation and bone
destruction occurs with balance more
towards bone formation, giving a more
radiopaque or sclerotic appearance.
 Bone pattern is granular.
 Scattered regions of radiolucency seen with
or without central sequestra.
 The affected maxillary bone may also be very
sclerotic and have areas of bone resorption.
 Effects on surrounding structures
 Inflammatory periosteal new bone
formation is uncommon, possibly because of
deleterious effects of radiation on
potential osteoblasts in the periosteum.
 Radiation exposure may stimulate the
resorption of bone, especially in Maxilla,
similar to appearance of bone destruction in
malignant lesion.
 Mostcommon effect on surrounding bone:
stimulation of sclerosis.
 MANAGEMENT
 Decorticationwith sequestrectomy, HBO
therapy with antibiotic therapy have shown
limited success.
 Conservative approaches with the aim of therapy
to maintain integrity of the lower border of the
Mandible and to keep the site free of infection,
and the patient free of pain, may in long term
prove more successful.
 Removal of teeth that have poor prognosis or
have significant periodontal disease before
radiation treatment and excellent oral and
denture hygiene are mainstays of preventive
treatment.
 FACTORS LEADING TO 116
OSTEORADIONECROSIS
 Irradiation of area of previous surgery before
healing occurs
 Irradiation of lesions in close proximity to bone
 High dose of radiation with or without proper
fractionation
 Combination of external radiation and intraoral
implants
 Poor oral hygiene and continue use of irritants
 Poor patient cooperation in managing irradiated
tissues 11
7

 Surgery in irradiated area

 Indiscriminate use of prosthetic appliances

following radiation therapy

 Failure to prevent trauma to irradiated bony

areas

 Presence of numerous physical and nutritional

problems prior to therapy
Steps to avoid Osteoradionecrosis
11
PRE THERAPY: 8

 All teeth with questionable prognosis should be extracted

 All restorable teeth should be restored.
 Thorough prophylaxis & topical fluoride application.
 Oral hygiene measures & instructions should be
demonstrated & reinforced.
 Any sharp cusps should be rounded to prevent mechanical
irritation.
 Impressions for fabrication of custom fluoride trays to be
used during treatment.
 Stop habits like tobacco use & alcohol consumption.
DURING THERAPY: 119

 Ptshould rinse mouth at least 10 time a day with

saline.
 Chlorhexidinemouth rinses twice daily to
minimize bacterial/ fungal levels within mouth.
 Weekly oral hygiene evaluation by dentist.
 Ifovergrowth of candida albicans – nystatin or
clotrimazole topical application.
 Monitor mouth opening.
 Monitor nutritional status.
POST THERAPY
120

 Dental evaluation every 3 – 4 months.

 Oral prophylaxis.

 Topical fluoride application should be done using custom

trays.

 Pt to be instructed in daily self administration of

topical fluoride administration.

 Salivary substitutes should be prescribed.

 121
 Restore teeth developing post-radiotherapy
caries using amalgam or composites.

 Extraction of teeth can be carried out with

the use of
- Hyperbaric oxygen before & after
extraction
- Prophylactic antibiotic

 Evaluate artificial dentures.

PERICORONITIS
PERICORONITIS
 Also known as operculitis.
 The term pericoronitis refers to
inflammation of tissues surrounding the
crown of a partially erupted tooth.
 Seencommonly in association with
mandibular third molars in young adults.
 The gingiva surrounding the erupted portion
of crown becomes inflamed when food debris
and microbial agents become trapped under
it.
 Thegingiva becomes secondarily
traumatized by opposing occlusion.

 Theinflammation may extend into

the bone surrounding the crown of
the tooth.
 Clinical features

 Pain and swelling.

 Trismus when third molar is affected.
 Ulcerated operculum is the source of
pain.
 Seen during the time of eruption of
third molars in young adults.
Radiographic features

Location:
 Bone changes, when present are centered
over the follicular space or the portion of
crown still embedded in bone or in close
proximity to bone.
 Mandibularthird molar region is the most
common location.
Periphery:
 Ill defined
 Gradual transition of the normal trabecular
pattern into a sclerotic region.

Internal structure:
 Adjacent bone is most often sclerotic with thick
trabeculae.
 Area of bone loss or radiolucency adjacent to
crown that enlarges the follicular space .
 If this lesion spreads, internal pattern becomes
consistent with osteomyelitis.
 Effects on surrounding structures:
 Typical
changes of sclerosis and
rarefaction of surrounding bone.
 Inextensive cases, periosteal new bone
formation may be seen at the inferior
cortex, the posterior border of ramus, and
along the coronoid notch of the mandible.
OSTEOSCLEROSIS
It is believed to be a reparatory process or a
compensatory process to stress

CLINICAL FEATURES

No associated signs and symptoms

RADIOGRAPHIC FEATURES

 It is seen as areas of dense bone

 They may be solitary, multiple,
unilateral or bilateral varying in size
from 2mm to 2cm in diameter having a
round or irregular shape
 Border may be distinct to indistinct,
ragged or blending to surrounding bone
 May arise around roots of tooth
subjected to masticatory forces
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